Abstract
Objective:Previous experiments have demonstrated that acute sleep loss impairs glucose homeostasis and increases food intake in humans. The incretin hormone glucagon-like peptide 1 (GLP-1) enhances postprandial insulin secretion and promotes satiety. Hypothesizing that the detrimental metabolic effects of sleep curtailment imply alterations in GLP-1 signaling, we investigated 24-h serum total GLP-1 concentrations during total sleep deprivation (TSD) and a normal sleep/wake cycle (comprising ∼8 h of sleep) in 12 healthy young men.Methods:Sessions started at 1800 h, and subjects were provided with standardized meals. Assessments of serum GLP-1 took place in 1.5- to 3-h intervals, focusing on the response to breakfast intake (3.8 MJ).Results:Across conditions, 24-h concentration profiles of GLP-1 were characterized by the expected postprandial increases (P<0.001). Although there were no differences in magnitude between conditions (P>0.11), the postprandial GLP-1 peak response to breakfast intake was delayed by ∼90 min following sleep loss in comparison with regular sleep (P<0.02).Conclusions:Results indicate that acute TSD exerts a mild, but discernible effect on the postprandial dynamics of circulating GLP-1 concentrations in healthy men.
Highlights
Epidemiological observations indicate that short sleep is associated with an increased risk to develop obesity and type 2 diabetes.[1,2] Respective experimental studies have provided evidence that acute sleep loss increases food intake[3,4] and impairs glucose tolerance and insulin sensitivity.[5]
Overall 24-h glucagon-like peptide 1 (GLP-1) concentrations were not affected, which might have been due to the subtlety of the intervention characterized by a slight shift from time spent in rapid-eye movement (REM) sleep to time spent in sleep stage 2.8
GLP-1 concentrations were not affected by total sleep deprivation (TSD) (P 1⁄4 0.83 for Sleep/TSD; P 1⁄4 0.11 for Sleep/TSD Â Time; 24-h mean, TSD vs Sleep, 39.1±12.1 vs 33.1±9.7 pmol l À 1; P 1⁄4 0.72; Figure 1a)
Summary
Epidemiological observations indicate that short sleep is associated with an increased risk to develop obesity and type 2 diabetes.[1,2] Respective experimental studies have provided evidence that acute sleep loss increases food intake[3,4] and impairs glucose tolerance and insulin sensitivity.[5]. Overall 24-h GLP-1 concentrations were not affected, which might have been due to the subtlety of the intervention characterized by a slight shift from time spent in rapid-eye movement (REM) sleep to time spent in sleep stage 2.8
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